Chronic lymphocytic leukemia (B-CLL) is the most common human leukemia in the world accounting for approximately 10,000 new cases each year in the United States.1 The TCL1 (T-cell leukemia/lymphoma 1) oncogene was discovered as a target of frequent chromosomal rearrangements at 14q31.2 in mature T-cell leukemias.2 Previously it was reported that transgenic mice expressing TCL1 in B-cells develop B-CLL.3 The inventor herein now believes that deregulation of TCL1 may be a causal event in the pathogenesis of B-CLL since the inventor has now also shown that TCL1 is a co-activator of the Akt oncoprotein, a critical molecule in the transduction of anti-apoptotic signals in B- and T-cells.4 
A recent report suggested that high TCL1 expression in human CLL correlates with unmutated VH status and ZAP70 positivity suggesting that TCL1-driven CLL is an aggressive form of B-CLL.5 One of the most significant genetic factors associated with poor prognosis in human B-CLL is the chromosome 11q deletion.6.
MicroRNAs are a large family of highly conserved non-coding genes thought to be involved in temporal and tissue specific gene regulation.7 We recently demonstrated that microRNA expression profiles can be used to distinguish normal B-cells from malignant B-CLL cells and that microRNA signatures are associated with prognosis and progression of chronic lymphocytic leukemia.8,9 
No universally successful method for the treatment or prevention of B-CLL is currently available. The course of treatment for is often selected based on a variety of prognostic parameters including an analysis of specific tumor markers.
In spite of considerable research into therapies for B-CLL, CLL remains difficult to diagnose and treat effectively, and the mortality observed in patients indicates that improvements are needed in the diagnosis, treatment and prevention of the disease.